Mouse intragastric infusion (iG) model

Southern California Research Center for ALPD and Cirrhosis, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
Nature Protocol (Impact Factor: 9.67). 04/2012; 7(4):771-81. DOI: 10.1038/nprot.2012.014
Source: PubMed

ABSTRACT Direct intragastric delivery of a diet, nutrient or test substance can be achieved in rodents (mice and rats) on a long-term (2-3 months) basis using a chronically implanted gastrostomy catheter and a flow-through swivel system. This rodent intragastric infusion (iG) model has broad applications in research on food intake, gastrointestinal (GI) physiology, GI neuroendocrinology, drug metabolism and toxicity, obesity and liver disease. It achieves maximal control over the rate and pattern of delivery and it can be combined with normal ad libitum feeding of solid diet if so desired. It may be adopted to achieve infusion at other sites of the GI system to test the role of a bypassed GI segment in neuroendocrine physiology, and its use in genetic mouse models facilitates the genetic analysis of a central question under investigation.

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    • "Lastly, we found that high fat diet (HCFD) present during Hybrid EtOH+Binge exposure aggravated the increase in P2X7R expression and activation status of astroglia. The iG ethanol exposure model in rodents was recently developed to aid in the investigation of the ethanol-induced liver damage (Tsukamoto et al., 2008; Ueno et al., 2012). Additional studies have reported a synergistic relationship between ethanol exposure and moderate adiposity such as found in the Hybrid paradigm in regards to causing liver damage (Deng et al., 2005; Xu et al., 2011). "
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    ABSTRACT: The present investigation tested the role of ATP-activated P2X7 receptors (P2X7Rs) in alcohol-induced brain damage using a model that combines intragastric (iG) ethanol feeding and high fat diet in C57BL/6J mice (Hybrid). The Hybrid paradigm caused increased levels of pro-inflammatory markers, changes in microglia and astrocytes, reduced levels of neuronal marker NeuN and increased P2X7R expression in ethanol-sensitive brain regions. Observed changes in P2X7R and NeuN expression were more pronounced in Hybrid paradigm with inclusion of additional weekly binges. In addition, high fat diet during Hybrid exposure aggravated the increase in P2X7R expression and activation of glial cells. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of neuroimmunology 06/2015; 285. DOI:10.1016/j.jneuroim.2015.06.007 · 2.47 Impact Factor
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    • "Various animal models have been developed to characterize pathological changes of ALD. In particular, two protocols have been developed in mice that mimic aspects of ALD development in humans: the Lieber-DeCarli alcohol liquid diet [11,12] and the Tsukamoto-French intragastric alcohol feeding protocol [13,14]. Animals on the Lieber-DeCarli liquid diet display significant liver lesions including steatosis, apoptosis, structural alteration of mitochondria and endoplasmic reticulum and corresponding changes like those found early in human ALD. "
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    ABSTRACT: Alcohol consumption is a major cause of liver disease in humans. The use and monitoring of biomarkers associated with early, pre-clinical stages of alcohol-induced liver disease (pre-ALD) could facilitate diagnosis and treatment, leading to improved outcomes. We investigated the pathological, transcriptomic and protein changes in early stages of pre-ALD in mice fed the Lieber-Decarli liquid diet with or without alcohol for four months to identify biomarkers for the early stage of alcohol induced liver injury. Mice were sampled after 1, 2 and 4 months treatment. Pathological examination revealed a modest increase in fatty liver changes in alcohol-treated mice. Transcriptomics revealed gene alterations at all time points. Most notably, the Igfbp1 (Insulin-Like Growth Factor Binding Protein 1) was selected as the best candidate gene for early detection of liver damage since it showed early and continuously enhanced induction during the treatment course. Consistent with the microarray data, both Igfbp1mRNA expression in the liver tissue and the IGFBP1 serum protein levels showed progressive and significant increases over the course of pre-ALD development. The results suggest that in conjunction with other tests, serum IGFBPI protein could provide an easily measured biomarker for early detection of alcohol-induced liver injury in humans.
    Journal of Translational Medicine 10/2013; 11(1):266. DOI:10.1186/1479-5876-11-266 · 3.93 Impact Factor
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    ABSTRACT: Chronic liver diseases are frequent and potentially life threatening for humans. The underlying aetiologies are divers, ranging from viral infections, autoimmune disorders, intoxications (including alcohol abuse) to imbalanced diets. Although at early stage of disease the liver regenerates in the absence of the insult, advanced stages cannot be healed and may require organ transplantation. A better understanding of underlying mechanisms is mandatory for the design of new drugs to be used in clinic. Therefore, rodent models are being developed to mimic human liver disease. However, no model to date can completely recapitulate the "corresponding" human disorder. Limiting factors are the time frame required in humans to establish a certain liver disease, rodents possess a distinct immune system compared to humans and have different metabolic rates affecting liver homeostasis. These features account for the difficulties in developing adequate rodent models for studying disease progression and for testing new pharmaceuticals to be translated into the clinic. Nevertheless, traditional and new promising animal models that mimic certain attributes of chronic liver diseases are established and being used to deepen our understanding in the underlying mechanisms of distinct liver diseases. This review aims at providing a comprehensive overview of recent advances in animal models recapitulating different features and aetiologies of human liver diseases.
    AJP Gastrointestinal and Liver Physiology 12/2012; 304(5). DOI:10.1152/ajpgi.00199.2012 · 3.80 Impact Factor
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